Abstract

In the global world diabetes and mitochondrial disease is expected to cost the developing world in the next 30 years US $400 million. In diabetes an absent peripheral sink amyloid beta clearance pathway is now relevant to amyloid beta induced mitochondrial apoptosis. The quality of food consumed has raised major concerns with increased levels of plasma bacterial lipopolysaccharides (LPS) that induces amyloid beta aggregation and mitochondrial apoptosis with programmed cell death linked to non alcoholic fatty liver disease (NAFLD) and many organ diseases. The amount, nature and time of day of fat consumption in diabetes has become important with relevance to caffeine metabolism, brain toxic amyloid beta oligomer formation and neuron apoptosis. To prevent programmed cell death dietary fat and caffeine consumption need to be revised to allow rapid hepatic caffeine and amyloid beta metabolism with the prevention of global mitophagy associated with diabetes, NAFLD and neurodegenerative diseases.